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Inhibition of Melanization by Kojic Acid Promotes Cell Wall Disruption of the Human Pathogenic Fungus Fonsecaea sp.
Chromoblastomycosis (CBM) is a chronic human subcutaneous mycosis caused by various aetiologic agents. CBM does not have an established treatment but may be managed using antifungal agents, surgical removal of the lesions, or cryotherapy. Kojic acid (KA), a known tyrosinase inhibitor with a variety...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9414132/ https://www.ncbi.nlm.nih.gov/pubmed/36015045 http://dx.doi.org/10.3390/pathogens11080925 |
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author | Pereira, Jorge Augusto Leão de Moraes, Lienne Silveira de Sena, Chubert Bernardo Castro do Nascimento, José Luiz Martins Rodrigues, Ana Paula D. da Silva, Silvia Helena Marques Silva, Edilene O. |
author_facet | Pereira, Jorge Augusto Leão de Moraes, Lienne Silveira de Sena, Chubert Bernardo Castro do Nascimento, José Luiz Martins Rodrigues, Ana Paula D. da Silva, Silvia Helena Marques Silva, Edilene O. |
author_sort | Pereira, Jorge Augusto Leão |
collection | PubMed |
description | Chromoblastomycosis (CBM) is a chronic human subcutaneous mycosis caused by various aetiologic agents. CBM does not have an established treatment but may be managed using antifungal agents, surgical removal of the lesions, or cryotherapy. Kojic acid (KA), a known tyrosinase inhibitor with a variety of biological actions, including fungistatic action against the fungus Cryptococcus neoformans, mediated by inhibiting melanin production, seems to be an alternative to improve the treatment of CBM. The aim of the present study was to analyze the action of KA against the pathogenic fungus Fonsecaea sp., an aetiological agent of CBM. The fungal culture was incubated with KA, and the amount of melanin was assessed, followed by cytochemical detection. Subsequently, the samples were analyzed by light microscopy, transmission and scanning electron microscopy. Culture analysis revealed that 100 g/mL KA significantly decreased the melanization of the fungus and the exocytosis of melanin into the culture supernatant. Additionally, KA induced less growth of biofilm formation and intense disruption of the cell wall, and decreased the number of melanin-containing vesicles in the culture supernatant. Finally, KA inhibited fungal filamentation in culture and the subsequent phagocytosis process. Thus, KA may be a promising substance to help in the treatment of CBM. |
format | Online Article Text |
id | pubmed-9414132 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-94141322022-08-27 Inhibition of Melanization by Kojic Acid Promotes Cell Wall Disruption of the Human Pathogenic Fungus Fonsecaea sp. Pereira, Jorge Augusto Leão de Moraes, Lienne Silveira de Sena, Chubert Bernardo Castro do Nascimento, José Luiz Martins Rodrigues, Ana Paula D. da Silva, Silvia Helena Marques Silva, Edilene O. Pathogens Article Chromoblastomycosis (CBM) is a chronic human subcutaneous mycosis caused by various aetiologic agents. CBM does not have an established treatment but may be managed using antifungal agents, surgical removal of the lesions, or cryotherapy. Kojic acid (KA), a known tyrosinase inhibitor with a variety of biological actions, including fungistatic action against the fungus Cryptococcus neoformans, mediated by inhibiting melanin production, seems to be an alternative to improve the treatment of CBM. The aim of the present study was to analyze the action of KA against the pathogenic fungus Fonsecaea sp., an aetiological agent of CBM. The fungal culture was incubated with KA, and the amount of melanin was assessed, followed by cytochemical detection. Subsequently, the samples were analyzed by light microscopy, transmission and scanning electron microscopy. Culture analysis revealed that 100 g/mL KA significantly decreased the melanization of the fungus and the exocytosis of melanin into the culture supernatant. Additionally, KA induced less growth of biofilm formation and intense disruption of the cell wall, and decreased the number of melanin-containing vesicles in the culture supernatant. Finally, KA inhibited fungal filamentation in culture and the subsequent phagocytosis process. Thus, KA may be a promising substance to help in the treatment of CBM. MDPI 2022-08-17 /pmc/articles/PMC9414132/ /pubmed/36015045 http://dx.doi.org/10.3390/pathogens11080925 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Pereira, Jorge Augusto Leão de Moraes, Lienne Silveira de Sena, Chubert Bernardo Castro do Nascimento, José Luiz Martins Rodrigues, Ana Paula D. da Silva, Silvia Helena Marques Silva, Edilene O. Inhibition of Melanization by Kojic Acid Promotes Cell Wall Disruption of the Human Pathogenic Fungus Fonsecaea sp. |
title | Inhibition of Melanization by Kojic Acid Promotes Cell Wall Disruption of the Human Pathogenic Fungus Fonsecaea sp. |
title_full | Inhibition of Melanization by Kojic Acid Promotes Cell Wall Disruption of the Human Pathogenic Fungus Fonsecaea sp. |
title_fullStr | Inhibition of Melanization by Kojic Acid Promotes Cell Wall Disruption of the Human Pathogenic Fungus Fonsecaea sp. |
title_full_unstemmed | Inhibition of Melanization by Kojic Acid Promotes Cell Wall Disruption of the Human Pathogenic Fungus Fonsecaea sp. |
title_short | Inhibition of Melanization by Kojic Acid Promotes Cell Wall Disruption of the Human Pathogenic Fungus Fonsecaea sp. |
title_sort | inhibition of melanization by kojic acid promotes cell wall disruption of the human pathogenic fungus fonsecaea sp. |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9414132/ https://www.ncbi.nlm.nih.gov/pubmed/36015045 http://dx.doi.org/10.3390/pathogens11080925 |
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